Epidermal Growth Factor Stimulates Transforming Growth Factor-Beta Receptor Type II Expression In Corneal Epithelial Cells.
Sci Rep
; 9(1): 8079, 2019 05 30.
Article
em En
| MEDLINE
| ID: mdl-31147562
ABSTRACT
We previously demonstrated that inhibition of epidermal growth factor receptor (EGFR) slowed corneal epithelial migration. Here we examine the effect of EGF on transforming growth factor-beta receptor II (TGF-ßRII) in a corneal wound-healing model and primary human corneal epithelial cells (pHCE). Corneal debridement wounds were made and allowed to heal ± Tyrphostin AG1478 (EGFR inhibitor), and assayed for EGFR activation and EGFR and TGF-ßRII localization. Primary HCE were treated with EGF ± U0126 (MEK inhibitor) and assayed for TGF-ßRII expression. EGFR activation was maximal 15 minutes after wounding and localized in the migrating epithelial cells. TGF-ßRII localization was also observed in the migrating epithelium and was reduced when EGFR was blocked. When pHCE were treated with EGF for 6 hours, the cells produced enhanced levels of TGF-ßRII, which was blocked by U0126. Downstream signaling pathways of MEK (p38MAPK and ERK1/2MAPK) were then examined, and TGF-ß1 and EGF were found to have differential effects on the phosphorylation of p38 and ERK1/2, with TGF-ß1 upregulating p-p38 but not pERK1/2 and EGF upregulating pERK1/2 but not p-p38. Taken together, these data indicate that EGF stimulates TGF-ßRII through ERK1/2 and EGFR signaling, suggesting interplay between EGF- and TGF-ß-signaling pathways during corneal wound repair.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Cicatrização
/
Epitélio Corneano
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Fator de Crescimento Epidérmico
/
Lesões da Córnea
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Receptor do Fator de Crescimento Transformador beta Tipo II
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article